Due to their pronounced capacity to prime T cells DC are considered as optimal tools to enhance insufficient T-cell responses against tumors. To initiate a specific cellular defence against tumors, tumor cells must be found wherever they are located in the body and must be recognized by tumor-reactive T lymphocytes, especially by CTL. The frequency of tumor-specific
CTL is usually extremely low and there is little evidence that antitumor immunity is efficiently induced in tumor-bearing hosts [31,32]. Possible reasons for this immune failure are: (1) the typically small amount of tumor-specific peptides presented as complexes with MHC molecules on tumor cells. (2) These antigens must be recognized by rare T cell clones through T cell receptors that (3) often have only a low affinity. (4) Tumor cells lack costimulatory molecules, that deliver additional signals required by naive T cells for primary activation. Recognition of antigen/MHC complexes in the absence of costimulation not only fails to activate T cells but may lead to a state of anergy . The main challenge is, therefore, to augment the frequency of active, tumor-specific CTL in order to produce an effective antitumor response in vivo and to overcome a possible state of specific anergy or tolerance. The use of DC as adjuvants for MHC class I-restricted antitumor response is a rather novel and particulary promising approach [34-36]. As mentioned above, DC are the only cell population known to date, that is effective to induce a primary response of CD4+ and CD8+ T cells. Once antigen-specific T cells have been activated they can respond to other cell types expressing the appropriate MHC-peptides without the specialized costimulatory signals delivered by DC.
to algorythms which are based on consensus anchor motifs for frequent HLA molecules. They are loaded on APC for in vitro stimulation of T lymphocytes . The tumor antigens described so far can be classified into six groups [41, 42], The first group represents tumor antigens encoded by genes that are silent in most normal tissues, except testis and placenta, but are expressed in a variety of different tumor types. Examples are the genes encoding MAGE [43, 44], BAGE , GAGE  and RAGE , These antigens are shared by different tumors and therefore represent promising targets for cancer immunotherapy. The second group comprises differentiation antigens, that are not only expressed in tumor cells but also in the corresponding normal cells. Examples are tyrosinase , Melan-A , gp 100  and CEA [51 ]. A third group contains antigens encoded by genes that are expressed ubiquitously but are mutated in tumor cells as e. g., CDK4 , /6-catenin  and bcr-abl [54, 55], The fourth category comprises antigens encoded by nonmutated genes, that are overexpressed in tumor cells such as Her-2/neu [56, 57] and p53 , The fifth group contains antigens, that derived from oncogenic viruses, like E6 and E7 of human papilloma virus  and a sixth group is represented by mucins , At present, the different types of tumor antigens are being evaluated in various strategies to activate antitumor T cells in vivo [61-63].
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